Evidence map›Paper›PMID 22289634›Full record

ArticleAging2012

TP53 codon 72 polymorphism affects accumulation of mtDNA damage in human cells.

Serena Altilia, Aurelia Santoro, Davide Malagoli, Catia Lanzarini, Josué Adolfo Ballesteros Álvarez, Gianluca Galazzo, Donald Carl Porter, Paolina Crocco, Giuseppina Rose, Giuseppe Passarino and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Journal of Cancer · 2019
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Molecular dynamics of the full-length p53 monomer.Cell cycle (Georgetown, Tex.) · 2013
    Article
  13. Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 2 countries.

Serena AltiliaDepartment of Experimental Pathology, University of Bologna, Bologna, 40126, Italy.
Aurelia Santoro
Davide Malagoli
Catia Lanzarini
Josué Adolfo Ballesteros Álvarez
Gianluca Galazzo
Donald Carl Porter
Paolina Crocco
Giuseppina Rose
Giuseppe Passarino
Igor Boris Roninson
Claudio Franceschi
Stefano Salvioli
University of Bologna · ITUniversity of Calabria · ITSenex Biotechnology (United States) · USUniversity of Modena and Reggio Emilia · ITUniversity of South Carolina · US

Funding

Secretory Patterns of Senescent Tumor CellsR01AG028687 · NIA · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RONINSON, IGOR B · 2007 to 2011
$1.6M
NIA NIH HHS R01 AG028687NIA NIH HHS R01AG028687
6 · The paper itself

Abstract

Human TP53 gene is characterised by a polymorphism at codon 72 leading to an Arginine-to-Proline (R/P) substitution. The two resulting p53 isoforms have a different subcellular localisation after stress (more nuclear or more mitochondrial for the P or R isoform, respectively). p53P72 variant is more efficient than p53R72 in inducing the expression of genes involved in nuclear DNA repair. Since p53 is involved also in mitochondrial DNA (mtDNA) maintenance, we wondered whether these p53 isoforms are associated with different accumulation of mtDNA damage. We observed that cells bearing p53R72 accumulate lower amount of mtDNA damage upon rotenone stress with respect to cells bearing p53P72, and that p53R72 co-localises with polymerase gamma more than p53P72. We also analysed the in vivo accumulation of heteroplasmy in a 300 bp fragment of mtDNA D-loop of 425 aged subjects. We observed that subjects with heteroplasmy higher than 5% are significantly less than expected in the p53R72/R72 group. On the whole, these data suggest that the polymorphism of TP53 at codon 72 affects the accumulation of mtDNA mutations, likely through the different ability of the two p53 isoforms to bind to polymerase gamma, and may contribute to in vivo accumulation of mtDNA mutations.

Indexed as

Polymorphism, Genetic8-Hydroxy-2'-DeoxyguanosineDeoxyguanosineDNA DamageDNA, MitochondrialGenotypeHCT116 CellsHumansProtein BindingProtein IsoformsProtein TransportTumor Suppressor Protein p538-Hydroxy-2'-DeoxyguanosineDeoxyguanosineDNA, MitochondrialProtein IsoformsTumor Suppressor Protein p53

Identifiers

PMID22289634
PMCPMC3292903
OpenAlexW1581288650

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.